Human Neutrophil Cytosolic Factor 1 (NCF1) interaction partners

A rare mutation in NCF1 encoding p47phox of the leukocyte NADPH oxidase (show NOX1 Antibodies) causes lack of superoxide generation, leads to chronic granulomatous disease and was recently (1200-2300 years ago) introduced into the Kavkazi Jewish population

Reduced carotid but not coronary artery atherosclerosis in patients with chronic granulomatous disease despite the high prevalence of traditional risk factors raises questions about the role of NADPH oxidase (show NOX1 Antibodies) in the pathogenesis of atherosclerosis.

Four novel mutations in the NCF1, NCF2 (show NCF2 Antibodies), and CYBB (show CYBB Antibodies) genees have been identified in chronic granulomatous disease patients in Morocco.

p47(phox) and Rac2 (show RAC2 Antibodies) accumulate only transiently at the phagosome at the onset of NADPH (show NQO1 Antibodies) activity and detach from the phagosome before the end of reactive oxygen species production.

two novel splice variants designed as NCF1-TV1 (retained intron 6) and NCF1-TV2 (retained part of intron 8)encoding two putative truncated proteins (239AA and 283AA). Two splice variants were up-regulated in the mastitis-infected cows' mammary tissues, blood and neutrophils compared with these of healthy cows.

A p47(phox) and Src kinase (show CSK Antibodies) activation of peroxide production by Nox2 (show CYBB Antibodies) appears to be an important contributor to vascular contractile mechanisms mediated through activation of protein kinase C (show PKC Antibodies).

Neutrophil Cytosolic Factor 1 (NCF1) Antigen Profile

Protein Summary

The protein encoded by this gene is a 47 kDa cytosolic subunit of neutrophil NADPH oxidase. This oxidase is a multicomponent enzyme that is activated to produce superoxide anion. Mutations in this gene have been associated with chronic granulomatous disease.